MATERIALS AND METHODS: This retrospective study included all pregnancies seen at the SLE Clinic, Kuala Lumpur Hospital from January 2008 to May 2020. Maternal outcomes included SLE flare during pregnancy, preeclampsia and eclampsia. Foetal outcomes included foetal loss, preterm birth and small-for-gestational age (SGA) neonates. Clinical and laboratory variables were examined. Variables from univariate analysis were entered into logistic regression model. Odds ratio and 95% confidence interval were reported.
RESULTS: Of the 131 pregnancies, 106 (80.9%) were live births. Twenty-six (24.5%) babies were born preterm and 35 (33%) neonates were SGA. Twenty-four (18.3%) women had disease flare during pregnancy, with the majority (22/24) being mild to moderate flares. Four women experienced preeclampsia while none had eclampsia. Predictors of adverse maternal outcomes included high SLEDAI-2K score, proteinuria and hypocomplementemia within 6 months before conception and during pregnancy; history of lupus nephritis (LN), pre-existing hypertension, antiphospholipid syndrome (APS), antiphospholipid antibodies, anti-Ro antibody and anti-RNP antibody. Predictors of adverse foetal outcomes comprised APS, preeclampsia, anti-Sm antibody, history of neuropsychiatric systemic lupus erythematosus (NPSLE) and azathioprine use.
CONCLUSION: Pregnancy in SLE women is best deferred until disease activity is in remission for at least 6 months before conception. A history of LN is associated with a 3-fold risk of renal flare during pregnancy. Haematological abnormalities are rare in disease flare during pregnancy.
OBJECTIVE: To determine whether any association exists between the finding of an increased thickness of placenta, abnormal placenta shape, placental calcification, placental lake and abnormal cord insertion site at 20-22 and 30-32 weeks gestation with an increased risk of uteroplacental complications or a poor pregnancy outcome.
METHODOLOGY: A real-time ultrasound was used at the time of detail scan (at 20-22 weeks gestation) and at 30-32 weeks gestation to look for placenta appearance, fetal growth and anomaly. The main outcome measures were risk of hypertension disease in pregnancy, fetal growth restriction and poor fetal outcomes such as low Apgar score and low cord pH.
RESULT: The majority of the participants were Malay (77.9%). Abnormal placenta found at both gestations were placental lakes and thickness, and only one case had marginal cord insertion. Approximately 6% of the cases were confirmed placenta previa. No abnormal shape or abnormal calcification found at both gestations. About 10% patient developed hypertensive disease in pregnancy, 15% of the fetus was found to have growth restriction and another 16% have low umbilical cord pH. Majority of them delivered at term (90%) and via vaginal delivery (81%). There was no significance between presence of abnormal placental lake and thickness at both gestations with the maternal and fetal outcome.
CONCLUSION: Presence of abnormal placental thickness and lakes at 30-32 weeks scan associated with maternal hypertensive disease, fetal growth restriction and low umbilical cord pH, however these were not statistically significant.
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